Archaeopteryx played a pivotal part in revealing one of the greatest transitions in the history of life when dinosaurs took to the skies and fluttered away. There are not many transitions that can quite rival that evolutionary moment but, if there is one, it is the journey that the terrestrial ancestors of whales made into the sea. How the largest mammals on the planet came to lead the lives that they do today is a matter that is much shrouded in mystery. More specifically, how the blue whale and its kin ended up filtering tiny organisms out of the water with fibrous baleen when they started with sharp and pointed teeth is a subject of tremendous debate. Now a new fossil find is doing for baleen whales what Archaeopteryx did for birds by providing the first glimpse of an animal that was in the midst of a remarkable transition.

To say that the origins of baleen are controversial is an understatement. One hypothesis suggests that teeth were lost during a suction-feeding stage of whale evolution and that baleen evolved thereafter. The other suggests that baleen evolved before teeth were lost. The new fossil solidly supports the second argument. The new species, named Coronodon havensteini, dates to the Oligocene epoch roughly 30 million years ago and has an astonishing mouth. While most of its teeth indicate that it captured large prey, its broad lower molars frame narrow slots that look like that had to have been used for filter-feeding. This notion is further supported by the fact that, structurally, the rest of specimen looks like an ancient relative of the filter feeding branch of the whale family. Given this, the researchers are arguing that filter-feeding was preceded by predatory feeding, and that suction-feeding (which is seen in a few whales) evolved separately within a group that was removed from modern baleen whales. You can read more in The Economist article that I wrote on this here.

That antibiotic use fuels the rise of resistance in bacterial populations is well understood. What is less well understood is where the antibiotic resistant genes come from in the first place. Some have argued that modern antibiotic resistant traits have evolved when bacterial populations come under intense selective pressure from drugs. Others have argued that antibiotic resistant traits have always been present in wild bacterial populations and that as human use of drugs has increased this has driven the distribution of these traits to dramatically rise. Now the discovery of a worryingly resistant bacterium from Antarctica is providing strong support for the argument that resistant traits have always been around.

Antibiotic contamination in Antarctica is almost nothing. Yes, it is possible that a bacterium from a more antibiotic contaminated region of the world could migrate there through the sea, the rain or human activity but this is widely viewed as unlikely. It is for this reason that the discovery of an unstoppable bacterium on the frozen continent is so surprising.

The species that has been found belongs to the genus Pseudomonas, the group that contains the highly troublesome Pseudomonas aeruginosa that routinely causes lethal resistant infections in nursing homes and hospitals. Yet, while P. aeruginosa is found all over the developed world and has had ample exposure to antibiotics over the years, the new species, creatively named 6A1, has never been seen by science before and appears to only occur in Antarctica.

If 6A1 was only resistant to one or two antibiotics, that would not be particularly noteworthy but this is not the case. The bug is resistant to a lot of antibiotics and extremely resistant to a number of the best drugs on the market today. I won't get into all the details here, but its resistance to the common antibiotics amoxicillin and cefoxitin was far greater than that seen in P. aeruginosa. Resistance to erythromycin was ten times greater than that seen in P. aeruginosa. Worse, against ertapenem, a state of the art last resort antibiotic, the new species proved 180 times more resistant than P. aeruginosa.

Let us all hope that 6A1 remains sequestered in Antarctica for a very very long time.

This research published online in Polar Biology and, while I could not weave it into the science section of The Economist, you can view the original peer reviewed paper here.

A new study is revealing that people are able to more quickly solve problems that test their ability to pay attention while standing up than when sitting down. This flies in the face of the long held notion that standing up requires us to pay a little bit of attention to keep our balance and that this, in turn, interferes with our ability to entirely pay attention to other matters. It is also this wrongheaded logic that has guided important exams to be taken sitting down. As it turns out, if we were take such exams standing up we'd probably perform better.

Academically, this finding suggests that a great many psychological experiments that have been conducted in the past would yield different results if participants in them were take engage in such experiments while sitting down. It will be interesting to see how the psychological community responds to this. You can read more in The Economist article that I wrote on this here,

Strains of antibiotic resistant tuberculosis are becoming more common and it is expected that nearly half of all cases of the disease will survive exposure to traditional front line drugs by 2050. This is driving an intense search for drugs that can bypass the resistances that are commonly seen arising in tuberculosis. Now a team is revealing that they have found a compound produced by another species of bacterium that regularly infects human lungs that looks like it has tremendous potential to control tuberculosis infections.

The compound in question is produced by the species Burkholderia gladioli. While exceptionally rare in most people, B gladioli thrives in the lungs of those suffering from cystic fibrosis. The reason the team behind the new research was attracted to this species is because, once it establishes itself in the lungs, it does an astounding job of making sure that no other bacteria encroach on its turf. This suggested that the species was producing compounds that had the potential to inhibit the growth of competition and this is precisely what the team discovered when they took a closer look. You can read more in The Economist article that I wrote on this here.

Six years ago a team revealed that the nests of birds that had cigarettes woven into them were less likely to contain blood sucking parasites than the nests of birds that did not have cigarettes in them. Further testing revealed that the nicotine content in the butts played a key part in keeping the parasites away. I wrote that up in Nature at the time and pointed out that the team behind the research did not really know if city birds were doing this by accident or had actually worked out that cigarettes were a valuable tool for use when parasites came to their nests. Now that same team is revealing evidence that the birds know perfectly well what they are doing.

Precisely why birds bring cigarettes to their nests is a matter of debate. Some argue that they collect discarded butts simply because they resemble natural materials like twigs while others argue that they know the butts repel parasites. To test out this latter idea, the team monitored house finch behaviour as they added either dead or living parasites to their nests. When live parasite numbers increased, female finches collected more butts for their nests than females that had dead parasites added. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

Cells sometimes intentionally kill themselves off even if they are not diseased are harmed. This often occurs during normal development (like the forming of fingers in embryos from an initially fin-like appendage). When cells die in this way, bits of them circulate and tell the immune system that their death has been an intentional and somewhat peaceful affair. This is staggeringly different from when cells die during infection. Under those circumstances, their dead fragments usually trigger a powerful immune response that creates intense inflammation. While initially useful, inflammation impairs healing if it lasts for too long. This has led to a lot of research into how inflammation can be better controlled with drugs. Now a team is revealing that they have found a way to do this by releasing compounds into the body that look an awful lot like the fragments of cells that intentionally killed themselves in a peaceful manner. You can read more in The Economist article that I wrote on this here.

Saw-scaled vipers are difficult to spot as they tend to be active at night, have venom that drives people to suffer catastrophic internal haemorrhages and live in places where medical care is limited. As such, it is not surprising that they kill an awful lot of people. Antivenoms are widespread and available where these snakes are found but a team of researchers studying survival data noticed that people were still often dying even if they got the antivenom in time. Concerned and confused, the researchers ran an analysis of antivenom performance against venom milked from a number of the vipers and discovered that many of the antivenoms on the market simply do not work in regions where advertising says they should.

Are we sure we have the right antidote on hand?

Image courtesy of Shantanu Kuveskar

The key issue at hand here is the fact that antivenoms are produced using venom and venom varies from snake to snake, sometimes even within the same species. So, if an antivenom is produced using a species of saw-scaled viper found in both India and Pakistan but only snakes from Pakistan have their venom collected for the creation of the drug, there is chance that the antivenom will not work very well (or at all) when used to treat snake bites in India. This is precisely what appears to have happened and the harm to people in Asia and Africa looks like it is quite significant.

Some of the antivenom companies that I spoke with were remarkably receptive to these findings. One clearly stated that they are going to re-label their bottles immediately so their drugs are only delivered to places where they do actually work. Another stated that they are going to start milking vipers from more regions to build better antivenoms. However, not all is rosy. One company flatly denied that they manufacture a very poorly performing antivenom that is advertised on their own website and another argued that the findings of the researchers were flawed. You can read more in The Economist article that I wrote on this here.

Cavities are one of the most problematic chronic oral diseases suffered by children and, for decades, the assumption has been that those who develop severe cavities largely have bad luck by inheriting genes that make their teeth vulnerable to the condition. Now a new study is revealing that this notion is nonsense.

The researchers behind the new work examined the role of genetics, environment, and disease on the composition of the bacteria and fungi that live in the mouth in a whopping 485 pairs of twins. They found that while there are several species of bacteria that are heritable (or prone to grow in mouths due to heritable conditions), these species play little or no part in the formation of cavities.

These findings prove that chronic cavities have to be almost entirely the result of bad eating behaviours and not down to inherited "bad" oral microbiology. On the larger scale, we are seeing loads of cardiovascular, immunological and respiratory diseases (including several cancers) that have strong connections to the composition of the bacterial bugs living in the gut. Some recent papers show that oral microbiota are important here too and, if that is so, then diet looks very important for preventing or controlling these diseases too while genetics look largely unimportant. You can read more in The Economist article that I wrote on this here.

In 2014, I reported a remarkable find in The Economist where researchers used a sleeping sickness drug to treat mice suffering from the rodent equivalent of autism. Administration of the drug, known as suramin, caused the autism traits to fade away over a matter of weeks. Similarly, as the drug treatment ended, the autistic traits came back. It was astonishing stuff but my editor and I were cautious in our reporting since what works in mice often does not work in men. Well, humans trials have now finished and the findings suggest that suramin has tremendous potential.

What works in mice is now working in men.

Image courtesy of Aaron Logan.

Like all first trials in humans, this one was small with just ten patients. All were autistic boys. Half were given a placebo and half were given suramin. The participants went through numerous tests throughout the treatment to monitor their behaviours and tease out whether the grip that autism had on them was weakened. All five of the kids who were given the suramin showed substantial gains while the drug was given while none of the children given the placebo did.

Obviously, this is a big deal since there is currently no drug available for treating autism but what these findings suggest from a biochemical perspective is perhaps even more important. Suramin gums up purine receptors on cells and prevents neurons (cells in the brain) in particular from entering what is known as the cellular danger response. While in this defensive mode, neurons become more resistant to a wide range of diseases but stop making connections with other neurons. This is not really a problem when someone is ill for a few days or weeks but the theory with autism is that patients with the condition have neurons that permanently get stuck in the danger response and can't stop responding to purine stimulation. The fact that suramin improves language and social skills in autistic patients while simultaneously decreasing repetitive behaviours suggests that the theory of the cellular danger response being a central cause of autism is likely correct.

This work has to be replicated before we can take it too seriously but the fact that what works in mice is working in autism sufferers is really something extraordinary. You can read more in The Economist article that I wrote on this here.

That people chronically exposed to severe air pollution develop lung diseases is entirely logical. However, what has been a conundrum is why such patients often succumb to heart disease. Some researchers have theorised that many of the tiny particles found in air pollution are capable of migrating from the lungs to the blood vessels around the heart but evidence for this has been extremely thin. Now a new study is revealing that this is absolutely true. Indeed, the findings are worse than anyone could have imagined, showing that pollutant particles are actually attracted to blood vessels suffering from the sort of inflammation that is typically caused by plaques that build up over years of unhealthy eating. You can read more in The Economist article that I wrote on this here.

Plastics carry a heavy environmental impact. While roughly 26% of plastic materials are recycled and 36% are burned for purposes of energy recovery, 38% end up lingering in landfills. While many attempts have been made to get various strains of fungi and bacteria to eat this junk, success has been limited due to the colossal amount of time that it takes these tiny organisms to chew plastic up. Now a new experiment is revealing that a far better way forward would be to put moth larvae to the task.

The team behind the new work thought up their experiment while they were studying the moth species Galleria mellonella which is fond of laying its eggs inside the hives of honey bees and chewing up beeswax. Since beeswax and plastic are structurally not too different, the researchers decided to put the larvae on plastic and monitor their behaviour. Remarkably, holes started to appear in 40 minutes. The authors are arguing that the discovery lays the basis for the development of biotechnological applications that could play a pivotal role in management of plastic waste and, frankly, I'm inclined to agree with them. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

We know from work done on mice raised in entirely sterile environments that an absence of healthy bacteria leads to changes in how the blood–brain barrier functions. This matters because the barrier plays a critical part in keeping out materials and pathogens that have no business hanging around in the brain. In contrast, administration of probiotics has been shown to restore both intestinal function and brain chemistry. Given these findings, researchers have speculated that concurrent treatment of probiotics while patients are taking antibiotics should ameliorate the damage caused by the antibiotics but evidence for this has been thin. Now a new study conducted in mice is revealing that this is something that is well worth further attention.

In the new work, researchers dosed baby mice with penicillin one week before birth and then continued giving it to them until they weaned. Throughout this process, they simultaneously monitored the bacteria in their guts, their behaviour and the integrity of their blood brain barriers. Remarkably, they found that, like mice raised in completely sterile environments, the antibiotic-treated mice had lasting changes in the bacteria found in their guts, modified blood brain barrier integrity and showed behavioural changes like increased aggression and reduced sociality. More importantly, they found that the use of probiotics partially prevented these negative effects. You can read more in The Economist article that I wrote on this here.

In his desperate search to magically extend his life, Qin Shi Huang sought out dragon's blood in the belief that if he could drink some, he would become immune to the illnesses of old age. Remarkably, a new study is now revealing that the blood of dragons truly does have the potential to cure disease.

Komodo dragons are mildly venomous but they also wield numerous pathogenic bacteria in their saliva. One bite is enough to trigger septic shock within hours in the large mammals that they eat. Thus, a common hunting tactic used by these predators is to bite a deer, back away and then slowly stalk the wounded animal until it falls. This intriguing strategy has raised questions over how the dragons survive with so many pathogenic species in their mouths - especially since dragons routinely bite one another during fights over territory and do not succumb to sepsis themselves. Now a new examination of their blood is revealing that they carry an armada of unique proteins that shield them from infection.

The team behind the new work identified forty-eight novel antimicrobial proteins. They then ran eight of the most promising looking ones through a series of bacterial exposure tests and found that seven showed serious potency against particularly menacing strains. Dragons appear to be born with the power to resist the very pathogens that they wield and, with a bit of work, it seems likely that we can wield this power too. You can read more in The Economist article that I wrote on this here.

While the water repelling properties of the lotus leaf are the stuff of legend, like much in nature, scientists have found a way to replicate them. Superhydrophobic surfaces (as lotus leaf mimicking materials are known) have been around for years and they do repel water very well but, to date, the lotus has always had a leg up on them. Scratch a lotus leaf and, while its water repelling nature will be temporarily lost, the tissues will heal and the water repelling trait will return. Scratch any superhydrophobic surface and the water repelling trait is permanently lost. Now a team has found a way to help these surfaces heal themselves by mimicking another living organism: the lizard. The researchers created multiple layers of water proof material that were sandwiched together using water soluble glue. When the top layers became compromised, water seeped in, dissolved the glue, drove the top layer to fall off and exposed the undamaged water proof layer below. The material literally sheds its skin like a reptile. You can read more in The Economist article that I wrote on this here.

In 1907 the Chicago Yellow Cab Company chose the colour of its cars based on a survey conducted at a nearby university. The survey showed that yellow was the most noticeable colour and led the company to infer that this would make it easier for potential passengers to spot their taxis in the sea of mass produced black cars prevalent at the time. Now, more than a century later, it turns out that yellow was a wise choice for a new study is revealing that taxis of that colour are much less likely to get into accidents than taxis of other colours.

The new work made use of a merger that took place between two taxi companies in Singapore during 2002. One of the companies used yellow cars and the other one used blue cars. Today, the company owns 4,175 yellow taxis and 12,525 blue ones.

The researchers analysed 36 months of detailed taxi, driver, and accident data that the taxi company supplied to them and found that there is an unquestionable link between colour and accidents. In total, yellow taxis had 6.1 fewer accidents per 1,000 taxis per month than blue taxis. That suggested that colour alone granted a 9% reduction in accident probability. The researchers found this hard to swallow so they set off to explore whether the driver populations had any significant differences. To do this, they analysed the demography and driving behavior of a random sample of 3,341 drivers for 3 months using 15 second interval location and status data from the taxis. This amounted to more than 150 million data points and showed that the drivers were driving nearly identically. Mechanical differences were also ruled out since the taxi company uses a single car model and all cars undergo the same service schedules.

This led the team to question whether yellow taxis were protected by simply being more noticeable than blue taxis. To test this idea, the researchers delved into detailed accident reports and looked for the nature of the accident and the lighting conditions in which it occurred. They theorised that if yellow had a protective effect, a yellow taxi would be less likely than a blue taxi to be involved in an accident when the taxi was clearly in the other driver’s view. This proved true. They also theorised that yellow would grant an even greater advantage at night since yellow has a stronger contrast than blue against a dark background. You can read more in The Economist article that I wrote on this here.

Pollinators are in trouble and ecologists are scrambling to try to keep populations healthy. Economically this matters since a serious decline in pollinators has the potential to doom much modern agriculture but, just in case the ecologists fail, engineers are getting ready to handle the problem. Interested in creating pollinators from tiny drones, a team of researchers has designed and synthesised ionic liquid gels that will allow pollen to stick and be transported artificially.

Honey bees get covered in pollen when they enter flowers to collect nectar and then drop that pollen off in other flowers as they forage. This pollination allows plants to sexually reproduce and is vital to their survival. To date, nobody has been able to find a substance similar to honey bee fur that could readily capture and release pollen grains but the researchers behind the new work suspected that they could manufacture such a substance with ionic liquid gels.

Ionic liquid gels are composed of electrolyte liquids trapped inside solid polymers. They are often electrically conductive, sturdy and have highly variable adhesive properties. This led the team to wonder whether it might be possible to create an ionic liquid gel that was sticky enough to collect pollen grains upon initial exposure to them but then capable of dropping the grains a minute later just as honey bee fur does as the insects rummage around inside flowers.

To test this idea out, the researchers used an acrylic to polymerise an imidazolium salt, which is well known to function as an effective ionic liquid, by baking a mixture of the materials in an oven at 80˚C. Once the ionic liquid gel formed, they measured its tackiness with a probe by monitoring how much load it took for the gel to adhere and how much load was needed for the gel to release the probe once it was stuck to it. This test revealed that the gel was able to rapidly adhere under a very light load but would then release just as quickly when the same small load was applied in reverse. Crucially, the gel did not lose its adhesive properties after multiple attach and release events.

Encouraged by these findings, the researchers applied the gel to horse hairs collected from paint brushes and then attached these hairs to their drones. They then manually piloted the drones to the flowers of the Japanese privet where they guided them to stick the hairs into the male and female organs of the plants. They studied the gel-coated hairs under the microscope between many of the flower visits and confirmed that they were getting coated in pollen. They then used fluorescent microscopy to confirm that pollination was indeed being initiated in the flowers that their drones visited. An abridged version of the research can be found in The Economist article that I wrote on this here.

While secrecy is common and consequential, there has been little research on it. Now a new study is revealing the sorts of secrets that people commonly keep. More importantly, it is revealing the first systematic analysis of how people experience the act of keeping a secret. As you can imagine, keeping secrets is hard work but whether having lots of secrets is actually harmful to our well being varies with how often we decide to think about them. You can read more in The Economist article that I wrote on this here.

Precisely what happens in the brain when we get drunk is still something of a mystery. This is largely because of the complex interactions between alcohol and the nervous system and one of the best ways of studying these interactions is to study the effects of alcohol on other animals. To this end a team of researchers ran a rather amusing experiment with juvenile crayfish. They found that, like many species, the crayfish were behaviourally sensitive to alcohol exposure and that they progressed through stages of intoxication that are strikingly similar to those seen in people. What came as an outright shock though was that the social history of the animals significantly modified the effects that alcohol had on them. Yeah, you read that right. Crayfish raised in tanks with many others got drunk far more quickly and became more dependent on alcohol than crayfish raised in isolation. The big question is whether social interactions during youth in people makes the brain vulnerable to alcohol in the same way. You can read more in The Economist article that I wrote on this here.

Chemical weapons are easy enough to detect with the right equipment but such equipment is often not at arm's reach when the use of such weapons is first suspected. Samples of contaminated surfaces need to be taken and run through detection devices and this takes valuable minutes. It would be better if soldiers could automatically detect the presence of dangerous compounds right when they are encountered and now a new system that integrates detection systems into a glove looks like it can grant this ability.

The new technology is a flexible glove with a tiny electro-chemical lab stitched into it that is designed to transmit its findings in real time to a nearby phone. The glove can, quite literally, sound the alarm by triggering an application installed on the phone to vibrate or beep. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do so here.

Read any geology textbook and it will tell you that winds only routinely transport sediment grains that are smaller than 2 millimeters in diameter. Thus, sand, silt and clay are all regularly moved around by wind but gravel, cobbles and boulders only get picked up by occasional fierce storms.

These rules have left geologists working in the Chilean desert perplexed by the discovery over the years of hundreds of mounds containing tens of thousands large crystal shards of the mineral gypsum. Many of the crystals are over 20 centimeters in length and clearly did not grow in the dry environment where they are being found. How the crystals got where they are has been a long standing mystery but now a new study is revealing the story of how they got there... tiny tornadoes that routinely pass through the area. You can read more in The Economist article that I wrote on this here. Alternatively, if you would like to hear me describe the research on The Economist's science podcast, you can do here.